阿尔茨海默病（AD）是一种常见中枢神经系统退行性疾病，脑内Aβ沉积诱发神经元凋亡是AD的主要发病机制。神经元可通过自噬促进Aβ清除，发挥抑制神经元凋亡的保护机制，而过度凋亡则会抑制自噬的发生，进而加速凋亡，可见凋亡和自噬的过程间存在交互作用。前期研究显示益肾化浊法具有良好的临床疗效，实验研究发现该法能减少SAMP8鼠脑内Aβ生成、保护神经元功能和调节突触可塑性。在此基础上，本研究拟采用SAMP8鼠为研究对象，以益肾化浊法复方及拆方为干预手段，从行为学、形态学与分子生物学角度，观察小鼠认知功能变化，神经元微观形态变化，“凋亡-自噬交互作用”过程中关键靶点的蛋白表达；结合观察神经元病理性凋亡和自噬清除Aβ情况，明晰该法配伍分层中“益肾”和“化浊”两部分在“抗凋亡”、“促自噬”中的特异性作用以及两者在复方系统内形成的“抗凋亡+促自噬”整体协同性效应，初步阐释其组方内涵，为临床应用提供实验依据。

Alzheimer’s disease (AD) is a common neurodegenerative disease, and the main mechanism is brain Aβ deposition toxicity leading to neuronal apoptosis. Neurons can clear Aβ by promoting autophagy to avoid apoptosis which functions in protective effect to inhibit neuronal apoptosis; while excessive apoptosis could suppress autophagy, thereby accelerating apoptosis, showing there was a crosstalk between apoptosis and autophagy. Pre-clinical studies have shown Yishen Huazhuo method has significant clinical effect, experimental studies have found that this method can reduce Aβ generation in SAMP8 mouse brain, protect neuronal function and regulate synaptic plasticity. Based on that, this study tries to uses SAMP8 as the research object, with compound and decomposed formula of YH method, through behavior, morphology and molecular biology, to observe changes in cognitive function, neuronal morphology changes, and key targets in the process of "crosstalk between apoptosis and autophagy"; binding observing pathological neuronal apoptosis and autophagy clearing Aβ, to investigate the specific role of the compatibility and separation function on “the anti-apoptotic" and "promoting autophagy "of "Yishen" and "Huazhuo" respectively, and the global synergistic effect of both within the compound formula " anti-apoptotic and promote autophagy", to preliminary interpret its prescription connotation, and to provide experimental evidence for clinical application.